How Mitochondrial Damage Affects Cell Function

James, Andrew M.; Murphy, Michael P.

doi:10.1159/000064721

Cited by 54 publications

(45 citation statements)

References 109 publications

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“…Hyperglycemia stimulates excess mitochondrial superoxide production, which has been shown to damage cells [47]. The mitochondria are themselves susceptible to Fig.…”

Section: •−mentioning

confidence: 99%

Diabetes-Induced Birth Defects: What Do We Know? What Can We Do?

Reece

2011

Curr Diab Rep

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Birth defects are the leading cause of infant mortality in the United States, which has one of the highest infant mortality rates in the developed world. Many of these birth defects can be attributed to pre-existing, or pregestational, diabetes in pregnancy, which significantly increases a mother's risk of having a child with a major birth defect. Strict preconceptional and early pregnancy glucose control, supplementation with multivitamins and fatty acids, and lower glycemic dietary management have been shown to reduce the incidence of birth defects in experimental and epidemiologic studies. However, because more than half of pregnancies are unplanned, these methods are not generalizable across the population. Thus, better interventions are urgently needed. Based on what we know about the molecular pathophysiology of diabetic embryopathy, our laboratory and others are developing interventions against to key molecular targets in this multifactorial disease process.

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“…Hyperglycemia stimulates excess mitochondrial superoxide production, which has been shown to damage cells [47]. The mitochondria are themselves susceptible to Fig.…”

Section: •−mentioning

confidence: 99%

Diabetes-Induced Birth Defects: What Do We Know? What Can We Do?

Reece

2011

Curr Diab Rep

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“…Sustained Ca 2+ release from the ER can trigger Ca 2+ uptake by the mitochondria. [227][228][229][230] The ability of mitochondria to buffer cytoplasmic Ca 2+ loads may be highly dependent on their energetic capacity, [231][232][233] and if unchecked, this process could potentially cause the MPT considering that Ca 2+ is a prototypical MPT inducing agent. 35,231 Conversely, small amounts of cytochrome c released from a sub-set of mitochondria in cervical carcinoma and pheochromocytoma cells reportedly functioned to alter ER Ca 2+ handling by binding inositol (1,4,5) trisphosphate receptors.…”

Section: Ros Rns Ca 2+ and Sphingolipids As Apoptosis Effectorsmentioning

confidence: 99%

Apoptosis effector mechanisms: A requiem performed in different keys

et al. 2006

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Apoptosis is the regulated form of cell death utilized by metazoans to remove unneeded, damaged, or potentially deleterious cells. Certain manifestations of apoptosis may be associated with the proteolytic activity of caspases. These changes are often held as hallmarks of apoptosis in dying cells. Consequently, many regard caspases as the central effectors or executioners of apoptosis. However, this "caspase-centric" paradigm of apoptotic cell death does not appear to be as universal as once believed. In fact, during apoptosis the efficacy of caspases may be highly dependent on the cytotoxic stimulus as well as genetic and epigenetic factors. An ever-increasing number of studies strongly suggest that there are effectors in addition to caspases, which are important in generating apoptotic signatures in dying cells. These seemingly caspase-independent effectors may represent evolutionarily redundant or failsafe mechanisms for apoptotic cell elimination. In this review, we will discuss the molecular regulation of caspases and various caspase-independent effectors of apoptosis, describe the potential context and/or limitations of these mechanisms, and explore why the understanding of these processes may have relevance in cancer where treatment is believed to engage apoptosis to destroy tumor cells.

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“…The accumulation of mitochondrial DNA mutations can cause cell dysfunction by altering oxidative phosphorylation and Ca 2+ homeostasis, inducing further oxidative stress and a defective turnover of mitochondrial proteins, and affecting the susceptibility to apoptosis [36]. In particular, the respiratory enzymes containing mutant mitochondrial DNA-encoded defective protein subunits exhibit impaired respiratory function and thereby increase the electron leak in the electron transport chain and ROS production, which in turn elevates oxidative stress and the damage to mitochondria [37].…”

Section: Mitochondrial Oxidative Dysfunction and Mitochondrial Dna Damentioning

confidence: 99%

Mitochondrial Dysfunction as an Initiating Event in Atherogenesis: A Plausible Hypothesis

Puddu

Galletti

et al. 2005

Cardiology

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It is now widely accepted that oxidant stress and the ensuing endothelial dysfunction play a key role in the pathogenesis of atherosclerosis and cardiovascular diseases. The mitochondrial respiratory chain is the major source of reactive oxygen species as byproducts of normal cell respiration. Mitochondria may also be important targets for reactive oxygen species, which may damage mitochondrial lipids, enzymes and DNA with following mitochondrial dysfunction. Free cholesterol, oxidized low-density lipoprotein and glycated high-density lipoprotein are further possible causes of mitochondrial dysfunction and/or apoptosis. Moreover, in patients with mitochondrial diseases, vascular complications are commonly observed at an early age, often in the absence of traditional risk factors for atherosclerosis. We propose that mitochondrial dysfunction, besides endothelial dysfunction, represents an important early step in the chain of events leading to atherosclerotic disease.

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How Mitochondrial Damage Affects Cell Function

Cited by 54 publications

References 109 publications

Diabetes-Induced Birth Defects: What Do We Know? What Can We Do?

Diabetes-Induced Birth Defects: What Do We Know? What Can We Do?

Apoptosis effector mechanisms: A requiem performed in different keys

Mitochondrial Dysfunction as an Initiating Event in Atherogenesis: A Plausible Hypothesis

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